Background

NO-sensitive guanylyl cyclase (NO-GC) is the most important receptor for NO. The NO signal is transmitted through an increase in cGMP to act on several effector molecules. The NO/cGMP cascade is involved in the regulation of vessel diameter ultimately contributing to set the blood pressure. Lack of NO or NO-GC is thought to alter the responsiveness of blood vessels as well as their composition. We hypothesize that arterial stiffness may be altered in the absence of NO-GC.

Methods

As arterial stiffness is an import indicator of cardiovascular risks and mortality, we aimed at determining the role of NO-GC for aortic stiffness using general KO mice (GCKO) and smooth muscle-specific KO mice (SMC-GCKO) for NO-GC. Measurement of pulse wave velocity (PWV) was frequently used to determine aortic stiffness. We used magnetic resonance tomography (17.6 Tesla) for non-invasive measurement of local aortic PWV. PWV was calculated by simultaneously measuring of cross-sectional change and volume flow in a defined time.

Results

Preliminary data indicate an increased PWV in GCKO mice whereas in SMC-GCKO, stiffness is unaltered. Aortic diameter was reduced in GCKO compared to WT whereas that in SMC-GCKO was not significantly different from controls. Global deletion of NO-GC did not affect cardiac output. These data will be correlated to structural data of aorta from these strains.

Conclusion

Deletion of NO-GC affects the physical properties of vascular tissue. This effect appears to be independent of hypertension.

Authors’ Affiliations

(1)

Physiologisches Institut, Universität Würzburg

(2)

Lehrstuhl für experimentelle Physik 5, Universität Würzburg

Copyright

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.